Clinical Ophthalmology
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Bilateral vision loss associated
with radiofrequency exposure
Dianna Liu
Franz Marie Cruz
Prem S Subramanian
Wilmer Eye Institute, The Johns
Hopkins School of Medicine,
Baltimore, Maryland, USA
Correspondence: Prem S Subramanian
Wilmer Eye Institute, Johns Hopkins
Hospital, 600 North Wolfe Street,
Baltimore, Maryland 21287, USA
Tel 1 410 955 8679
Fax 1 410 614 9240
Email psubram1@jhmi.edu
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http://dx.doi.org/10.2147/OPTH.S38783
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C A S E R E P O RT
This article was published in the following Dove Press journal:
Clinical Ophthalmology
11 December 2012
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Abstract: A 57-year-old otherwise healthy woman presented with painless binocular vision
loss 1 week after direct application of radiofrequency energy to her orbits. She had no light
perception bilaterally. Pupils were dilated and not reactive to light. Fundoscopic exam initially
showed optic disc swelling in the right eye and a normal-appearing disc in the left eye. Magnetic
resonance imaging of the brain and orbits showed gadolinium enhancement of both intraorbital
optic nerves. She underwent a course of high-dose steroid treatment without recovery of vision.
Optic discs were pale 11 weeks after injury. With exclusion of other possible causes, this rep-
resents a unique case of irreversible binocular optic nerve damage and blindness secondary to
radiofrequency exposure.
Keywords: optic neuropathy, blindness, radiofrequency, vision loss
Radiofrequency radiation (RFR) is a form of electromagnetic radiation at frequencies
ranging from 3 kHz to 300 GHz. Several household appliances emit RFR, including
the television, radio, microwave oven, and cellular phones. In medicine, RFR is emit-
ted by diathermy equipment, electrocautery devices, magnetic resonance imaging
(MRI) scanners, and hyperthermia devices for cancer treatment. RFR causes damage
by heating body tissues, producing protein denaturation, cell membrane disruption,
and cell death.1
Few papers report optic nerve damage as the result of RFR.2–5 Monocular blindness
resulted as an immediate complication of trigeminal RF rhizotomy for the treatment
of trigeminal neuralgia. Visual loss has also been reported following the use of elec-
trocautery probes to achieve hemostasis in orbital and sinus surgeries. 4,5 Conflicting
data exist on the induction of cataract in humans (primarily radar operators) by low-
level chronic RFR exposure.6 We report on a case of binocular blindness from RFR
exposure for alternative medical therapy.
Case report
A 57-year-old Asian female with no significant past medical history presented to the
neuro-ophthalmology clinic with visual loss in both eyes. Family medical history
was unremarkable. She was a moderate (6.00 D OU) myope. About 18 months
before presentation, the patient was collecting rocks in stagnant water and soon
thereafter developed a sensation of tapeworms in her scalp. She was seen by mul-
tiple local dermatologists; no parasites were ever identified. She was diagnosed
with delusional parasitosis and was advised psychiatric evaluation. She reported
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which permits unrestricted noncommercial use, provided the original work is properly cited.
Liu et al Dovepress

seeing white spaghetti strands of worms across her face

and hearing the movement of the worms in her ears. She
had acquired mebendazole tablets from Hong Kong and had
been self-administering the drug on an intermittent basis.
She had also tried topical treatments with chemicals, such
as turpentine.
When none of these alleviated her symptoms, she
acquired a ProGen II 4050 frequency generator (Resonant
Light Technology Inc, Courtenay, British Columbia, Can-
ada) for bioelectronic therapy, which claims to kill microor-
ganisms. She applied the contact pads on her scalp several
times. Feeling that immature worms were in her eyelids and
lashes, she applied the contact pads (38  88 mm) directly
over her eyelids for a single treatment of each eyelid, during
which the generator output ranged between 90 to 580 kHz
for about 30 seconds at 14 volts. She did not recall the pulse
frequency. She had the contact pads in place for 10 minutes
on her left and 15 minutes on her right eye. During that time
she reported no pain or heat. She felt only the pulsations
“beating her eyelids.” No pressure was applied to the eyelids
to hold the patches in place.
The following day she noted blurred vision in both eyes,
which she described as “snowy.” She had no pain with eye
movement, redness, photosensitivity, or transient visual
obscurations. She denied any headache, fever, numbness,
weakness, or paresthesia. Over the next week, her vision
slowly worsened to complete blindness. She was admit-
ted to a local hospital where computed tomography (CT)
of the head showed moderate atrophic changes in both
frontal lobes. Orbital CT demonstrated myopic globes
without any mass. Magnetic resonance imaging (MRI) of
the brain and orbits with gadolinium contrast showed T2
hyperintensity in the right optic nerve (Figure 1). Cranial
magnetic resonance (MR) venography was unremarkable.
Erythrocyte sedimentation rate (ESR) was 7 mm/hour and
C-reactive protein (CRP) , 0.1 mg/L. Additional work-up to Figure 1 Orbital MRI T2-weighted sequences demonstrating hyperintensity in the
posterior aspect of the right optic nerve (arrows). Hyperintensity is seen in both
exclude autoimmune, nutritional, and inflammatory causes axial (A) and coronal (B) images.
of bilateral vision loss, including complete blood count Abbreviation: MRI, magnetic resonance imaging.
with platelet count, antinuclear antibody (ANA), antibody
markers for neuromyelitis optica, Lyme disease and syphilis, perception in each eye. The pupils were 6 millimeters and
serum levels of vitamin B12 and folic acid, and chest CT nonreactive to light. They constricted on convergence effort.
were normal or negative. She was diagnosed with bilateral Extraocular muscle movements were full. Anterior chambers
retrobulbar optic neuritis and treated with 5 days of 1 gram were deep and quiet. She had mild nuclear sclerotic cataracts
IV methylprednisolone with a tapering dose of oral predni- in both eyes; intraocular pressures were normal. The right
sone starting at 60 mg/day. optic nerve was swollen, while the left optic nerve was tilted
She presented to our clinic 3 weeks after onset of visual with peripapillary atrophy (Figure 2). Both optic nerve heads
loss. On ophthalmic examination, visual acuity was no light were hyperemic. The retinal vasculature, especially the

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Clinical Ophthalmology 2012:6
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Figure 2 Fundus photos at presentation. (A) optic disc swelling in the right eye and
(B) a tilted optic disc with peripapillary atrophy in the left eye.
arterioles, was markedly attenuated in both eyes. There was
an inactive chorioretinal scar anterior to the inferior arcade
in the right eye. No retinal hemorrhages, exudates, or cotton
wool spots were appreciated.
Fluorescein angiogram of the right fundus showed delayed
filling of the choroid and retina and late dye leakage from the
optic disc. Late images of the left fundus did not show any
abnormal leakage, staining, or capillary nonperfusion. No
further treatment was recommended aside from psychiatric
consultation, which the patient refused.
She returned after 8 weeks. Repeat examination
revealed vision remained to be no light perception. There
was diffuse optic nerve pallor of the right eye more than
Clinical Ophthalmology 2012:6
Bilateral vision loss associated with radiofrequency exposure
Figure 3 Optic disc appearance about 3 months after radiofrequency radiation
injury. Diffuse optic disc pallor is shown in both eyes with (A) resolving right optic
disc swelling and (B) marked arteriolar attenuation.
the left (Figure 3). The retina exhibited marked arteriolar
narrowing. On 3 month follow-up, the patient’s vision loss
was unchanged and there were no significant changes to her
health. She continued to deny any systemic symptoms.
Discussion
We present a patient with subacute, painless, binocular,
complete vision loss after orbital RFR exposure. Disc
swelling with dye leakage on fluorescein angiography
was present in the right eye, while the left eye had a
normal-appearing disc. Gadolinium-enhancement and T2
hyperintensity of the optic nerves were appreciated on
the MRI.
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Liu et al
Sudden monocular blindness has been reported as a result
of trigeminal RF rhizotomy in the treatment of trigeminal
neuralgia.2,3 In these cases optic nerve damage resulted from
misdirection of the stylet to the inferior orbital fissure and
into the optic canal where it was in contact with the optic
nerve. In three of four reported cases wherein immediate
ophthalmologic referral and assessment were made, fundos-
copy revealed normal-appearing optic discs. Pathology of
the optic nerve from one of these cases revealed edematous
axonal fibers and coagulation necrosis with focal areas of
acute hemorrhage compatible with thermal injury to the optic
nerve 2–3 cm behind the globe.3
Irreversibility of vision loss in our patient suggests that
there was axonal injury rather than pure demyelination, just
as was seen in the rhizotomy cases. A purely demyelinating
process may be reversible. Electrocautery can cause variable
degrees of demyelination.5 In a case report, it was shown that
blindness from electrocautery use during orbital surgery was
reversible, with the patient regaining 20/40 vision from no
light perception 10 weeks after surgery.
While the case reports we have mentioned involved
direct contact of the optic nerve with the RF-generating
instrument, RF energy can penetrate deeper into the body
and cause heating of remote tissues or organs.1 For example,
monocular blindness has been reported following electroco-
agulation during sinus surgery,4 although even in this case
the instrument was directly adjacent to the optic canal. In
our case, the RF source was between 5 and 25 mm from the
injured tissue (retinal ganglion cell layer), which is quite
different from previously reported cases. We thus postulate
that thermal injury can occur without direct contact with
the instrument, which is likely what happened to the patient
we have reported as the RF application occurred on the
eyelids. Thermal injury to the retinal ganglion cells might
occur though disruption of axonal ultrastructure, including
microtubules,7 which would result in the subacute vision loss
noted by this patient. Direct thermal injury and occlusion of
the retinal and/or optic nerve vasculature is much less likely
to have occurred because immediate severe vision loss would
be expected in that case.
Other possible causes of this patient’s vision loss include
Leber’s hereditary optic neuropathy (LHON), which can
cause subacute, simultaneous, painless, bilateral, profound
vision loss but rarely gives no light perception. Although
LHON is more common in men, the rate of vision loss
among women at risk ranges from 8% to 32%.8 LHON in
the acute stage is also characterized by the triad of fundus
findings, including pseudoedema of the peripapillary nerve
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fiber layer, circumpapillary telangiectatic microangiopathy,
and absence of disc leakage on fluorescein angiography. True
optic disc edema with documentation of optic disc leakage on
fluorescein angiography in our patient points against LHON
as the diagnosis.
Although arteritic ischemic optic neuropathy (AION)
from giant cell arteritis (GCA) has been reported to be
associated with optic nerve enhancement with gadolinium
on MRI,9 vision loss from bilateral simultaneous AION was
unlikely due to absence of other systemic symptoms of GCA.
The optic discs did not exhibit the typical pallid swelling of
AION. ESR, CRP, and platelet count were not elevated, and
the patient’s age also makes GCA less likely.
Neuromyelitis optica (NMO) may cause bilateral, simulta-
neous, severe optic neuritis with poor visual recovery. While
a negative NMO immunoglobulin G (IgG) test does not rule
out NMO, our patient fails to meet the diagnostic criteria for
NMO, which requires not only optic neuritis but also transverse
myelitis plus two of three of the following: NMO IgG seroposi-
tivity, longitudinally extensive transverse myelitis on imaging,
and a brain MRI not suggestive of multiple sclerosis.10
Nutritional optic neuropathy is usually characterized
by slowly progressive, bilateral visual decline. Total vision
loss is also unusual in nutritional optic neuropathy.11 Normal
vitamin B12 and folate levels further exclude nutritional
optic neuropathy as the cause of our patient’s vision loss.
Other causes of bilateral optic neuritis, including sarcoidosis,
syphilis, and Lyme disease, were excluded by negative labo-
ratory test results. Optic neuropathy in these cases is typically
associated with pain and may show a dramatic response to
steroids. Infiltrative optic neuropathy, particularly meningeal
carcinomatosis, may cause subacute, profound, bilateral
vision loss. However, this seems unlikely due to the absence
of other neurological signs or MRI findings.
Visual loss by thermal injury following RF exposure is
rare. Without tissue analysis, the diagnosis of RFR-induced
optic neuropathy is made by exclusion of other entities. We
encourage physicians to inquire about RFR-generating device
use in patients with optic neuropathy in whom the cause of
the vision loss may be elusive.
Acknowledgments
This research was supported in part by an unrestricted
grant to the Wilmer Eye Institute from Research to Prevent
Blindness, Inc, New York, NY, USA.
Disclosure
The authors report no conflict of interest in this work.
Clinical Ophthalmology 2012:6
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